The Amygdala, a component of the limbic system in the brain, is a set of subcortical nuclei that is important in decoding emotions such as fear and anxiety. The amygdala facilitates symptoms of anxiety (anxiogenic), when input signals of potential danger are received. These symptoms of anxiety help the organism protect itself from the posing threat. In the brain there seems to exist structures that act like a brake to the amygdala, inhibiting symptoms of anxiety (anxiolytic), and have a reciprocal relationship with the amygdala, such as the septum and the medial prefrontal cortex. The purpose of this research is to provide further evidence of the role of the medial prefrontal cortex, a structure thought to have similar anxiolytic effects as the septum, in the inhibition of the amygdala.

We propose the neurotransmitter possibly responsible for inhibition in the amygdala is the neurotransmitter GABA. When GABA binds to its receptor, chloride ions are able to pass through the chloride channel and provide the anxiolytic effect to the amygdala. If picrotoxin, a competitive antagonist at the GABA receptor is injected into the animal, the anxiolytic effect which GABA provides will be blocked. Animals will be fixed with the appropriate electrodes by stereotaxic technique. Stimulation to the medial prefrontal cortex is achieved by a series of 10ms monophasic pulses to the medial prefrontal cortex.

The role the medial prefrontal cortex can be understood by assessing activity in the amygdala when stimulation occurs in the medial prefrontal cortex. We expect activity in the amygdala will decrease when the medial prefrontal cortex has been stimulated. The effect of stimulation on cellular activity will be assessed by comparing the effect of the presence and absence of picrotoxin and then assessing the effect of stimulation to the medial prefrontal cortex. If similar results are found in the medial prefrontal cortex as in the septum, a better understanding of the effect fear and anxiety have on the brain can be established.